PSSM1 - The Sugar Storage Crisis: Understanding the Genetic Foundation and Management Strategies

PSSM1 represents one of the clearest examples of how a single genetic mutation can disrupt cellular function and how targeted nutrition can restore balance. This condition demonstrates the principles that apply across all muscle disorders: identify the specific dysfunction, understand its cellular effects, and provide precise nutritional support.

The PSSM1 mutation affects the GYS1 gene, which produces glycogen synthase 1—the enzyme responsible for building glycogen, the stored form of glucose that muscles use for quick energy. This seemingly small genetic change creates a cascade of metabolic problems that can devastate athletic performance.

In healthy horses, glycogen synthase functions like a thermostat in your home, turning on when energy storage is needed and shutting off when adequate glycogen reserves are present. The PSSM1 mutation breaks this regulatory system—the "thermostat" gets stuck in the "on" position, causing the enzyme to continuously produce glycogen regardless of the cell's actual storage needs.

This creates a double problem: not only do cells become packed with excessive glycogen, but the glycogen produced has an abnormal structure that makes it difficult to break down when muscles actually need energy. It's like having an overstuffed storage room where items are poorly organized and hard to retrieve when you need them.

The PSSM1 mutation disrupts normal cellular function in several specific ways:

·        Overproduction: Cells pack with glycogen even when they don't need it, like a refrigerator that keeps making ice even when the ice bin is already overflowing. This excess glycogen takes up space that should be available for normal cellular functions and can interfere with muscle fiber mechanics.

·        Poor quality: The glycogen produced has abnormal branching patterns, similar to a tree with too few branches. Normal glycogen has many branch points that provide multiple access sites for enzymes to quickly release glucose. PSSM1 glycogen has fewer branches, making it much harder for the muscle to access stored energy efficiently.

·        Access problems: Even though muscles are packed with stored energy, they struggle to break down this abnormal glycogen quickly enough during exercise. It's like having a full gas tank but a clogged fuel line—the energy is there, but it can't get where it needs to go fast enough to meet demands.

·        Insulin sensitivity: Many PSSM1 horses become hypersensitive to insulin, the hormone that signals cells to store glucose as glycogen. This means that even small amounts of sugar or starch in their diet trigger excessive insulin release, which drives even more glycogen production and worsens the storage problem.

Recognizing PSSM1 in the Field

These horses typically have a distinctive presentation that becomes unmistakable once you know what to look for.

Classic Presentation: These horses often look like they should be superstars. They typically have excellent muscle mass, good conformation, and seem to possess all the physical attributes for athletic success. The disconnect between appearance and performance is often the first clue.

The Episode Pattern: PSSM1 episodes follow predictable triggers that owners can learn to recognize and prevent such as:

·        Tying-Up: Episodes often occur after rest days when glycogen has accumulated in muscle cells. Horses that are fine on Sunday may tie up on Wednesday when returning to work after few days off.

·        Feed-related episodes: High-sugar or high-starch meals (like conventional grain-based diets) trigger insulin release, which drives more glycogen production and can precipitate episodes within hours of eating grain. sweet feeds, or fresh grass.

·        Stress responses: Transportation, competition, or environmental changes increase stress hormones that can trigger episodes. Many PSSM1 horses tie up during or after trailering to shows or when their routine is disrupted.

·        Weather sensitivity: Cold weather often worsens symptoms, possibly due to increased energy demands for maintaining body temperature or stress from environmental changes.

Subtle Early Signs to Watch For: Many PSSM1 horses show warning signs before developing full blown episodes. Learning to recognize these early indicators can prevent serious issues:

·        Shortened stride that doesn't improve with warm-up - The horse moves with a choppy, restricted gait that stays the same even after 20-30 minutes of walking and light work.

·        Reluctance to engage the hindquarters or collect - The horse resists moving forward from the hindquarters, feels "stuck" behind, or cannot maintain collection that was previously easy.

·        Excessive sweating during routine work - The horse sweats heavily during exercise that should be well within their fitness level, indicating their muscles are working much harder than they should.

·        Changes in attitude or willingness under saddle - A previously cooperative horse becomes reluctant, cranky, or resistant to work, often indicating discomfort they cannot express otherwise.

·        Stiffness that persists hours after exercise - Instead of cooling out normally, the horse remains stiff and uncomfortable for several hours or even into the next day after routine work.

Crisis Presentations: When PSSM1 horses experience episodes, the symptoms are dramatic and require immediate veterinary attention:

·        Rock-hard, painful muscles, especially in the hindquarters - The muscles feel like concrete under your hand and are extremely painful to touch. Horses often stand with a "sawhorse" stance, trying to relieve pressure on affected muscles.

·        Dark red or coffee-colored urine (myoglobinuria) - Damaged muscle tissue releases proteins into the bloodstream that are filtered by the kidneys, turning urine dark brown or red. This indicates severe muscle breakdown.

·        Profuse sweating and obvious distress - The horse sweats heavily and shows clear signs of pain including rapid breathing, pawing, or looking at their flanks. They appear anxious and uncomfortable. Similar to colic symptoms.

·        Reluctance or inability to move - Horses may refuse to walk, move with extreme stiffness, or in severe cases be unable to move at all. Even gentle encouragement to walk forward may be met with resistance.

·        Dramatic elevation in muscle enzymes - Blood tests show creatine kinase (CK) levels often reaching 5,000-15,000 U/L (normal is under 300), indicating massive muscle damage requiring immediate treatment.

The Management Revolution  

PSSM1 management requires throwing out conventional feeding wisdom and embracing a completely different approach.

The Old Way (That Failed):

• High-grain diet for energy and condition.

• Alfalfa hay for protein and calories.

• Sweet feeds and molasses for palatability.

• Rest days for recovery

The New Way (That Workes):

• Carbohydrate restriction to less than 10% of diet

• Healthy fat supplementation for energy replacement

• Daily exercise requirement (no complete rest days)

• Stress reduction and routine optimization

  
  

  Nutritional Protocol That Changes Everything

  
  

  Phase 1: The Dietary Overhaul (Days 1-30)

  This critical first phase focuses on stopping the glycogen overproduction that drives PSSM1 episodes. Every carbohydrate source must be evaluated and most eliminated to give the horse's system a chance to reset. Essentially PSSM1 requires the equine equivalent of a ketogenic diet.

  
  

  Carbohydrate Restriction: Total non-structural carbohydrates (NSC) below 10% - This includes all sugars and starches from every source in the diet. You'll need to calculate the total NSC from hay, any remaining feeds, and treats to ensure you stay under this crucial threshold.

  Eliminate all grain-based - Remove wheat, oats, corn, barley, sweet feeds, pelleted feeds, and any grain-containing products. Even "low-starch" commercial feeds often contain too many carbohydrates for PSSM1 horses during this critical phase.

  Choose tested hay with NSC below 12% - Have your hay analyzed for sugar and starch content, as NSC levels can vary dramatically even within the same cutting. Late-cut, mature hay typically has lower NSC than early-cut, leafy hay. This is the WSC + Starch = NSC. It should ideally be below 10% or lower, in my professional opinion.

  Remove all treats containing sugar or starch - This means no apples (although Granny Smiths can be safe), carrots, commercial horse treats, sugar cubes, molasses-based treats, or grain-based rewards. Even small amounts can trigger episodes in sensitive horses. StableFeed makes some excellent chia biscuit options that are safe for PSSM1 horses.

  Feed only what's absolutely necessary - During the critical or “active” phase, many horses receive only tested low-NSC hay, a vitamin/mineral supplement, and essential nutrients like vitamin E and magnesium. This may seem restrictive, but it's temporary and crucial for breaking the glycogen overload cycle.

  
  

Monitor body condition carefully - These whole food fat sources provide concentrated energy, so horses often maintain or gain weight on smaller volumes of feed than we're accustomed to. Adjust quantities based on the horse's condition and energy needs.

Ensure freshness and quality – Organic, unprocessed, without additives or preservatives whenever possible.

Essential Support Nutrients:

• Vitamin E

• Selenium: based on regional status

• Magnesium Glycinate or Magnesium Malate

• B-vitamin complex emphasizing thiamine

Key Principles for feeding PSSM1:

• Multiple small meals throughout the day

• Consistent timing to support metabolic rhythms

• High-quality forage with low NSC as the foundation

• Gradual introduction of fat sources

The Exercise Prescription That Makes the Difference

Exercise isn't just beneficial for PSSM1 horses—it's absolutely essential. Even on days when we didn't plan to work them, they need movement to prevent glycogen accumulation. Now, that doesn’t mean intense or strenuous work, just movement.

The Non-Negotiable Rule: PSSM1 horses must move every single day. This doesn't necessarily mean formal training, but they need a minimum of 30-45 minutes of working walk to help utilize stored glycogen and improve metabolic flexibility.

Example Progressive Exercise Protocol:

Weeks 1-4: Foundation Building

• Daily walking: 30-45 minutes minimum

• Surface: firm, even footing preferred

• Pace: working walk (approximately 4 mph)

• Goal: establish movement habits and assess tolerance

  
  

Weeks 5-8: Adding Some Intensity

• Continuing daily walking requirement

• Add short trotting intervals: 5-10 minutes in total time

• Include gentle hills for very short periods to incorporate strength building

• Monitor for any signs of regression and stop IMMEDIATELY if the present

Weeks 9-12: Sport-Specific Development

• Extend trotting periods to 15-20 minutes in total time

• Begin sport-specific exercises

• Maintain 70% of work at aerobic intensities

• Regular assessment and adjustment

Example Weekly Schedule (After 3 months):

• Monday: 60 minutes trail ride

• Tuesday: 45 minutes arena work with lateral exercises

• Wednesday: 90 minutes long-line work

• Thursday: 60 minutes driving practice

• Friday: 45 minutes trail ride

• Saturday: Competition or longer training session

• Sunday: 60 minutes walking (never a complete rest day)

The Monitoring System That Prevents Setbacks

One of the biggest mistakes I see with PSSM1 management is assuming that initial improvement means the horse is "cured." These horses require lifelong management, and subtle changes in their condition often predict problems before they become crises. I always recommend clients keep a daily log with documentation of what was done, and any observations they had during their exercise session. (Exercise session = ride, ground work, etc.)

Daily Assessment Protocol:

• Morning attitude and movement evaluation

• Pre-exercise willingness and comfort

• Post-exercise recovery

• Appetite and water consumption monitoring

Monthly Monitoring:

• Body condition scoring and muscle development tracking

• Exercise tolerance evaluation

• Muscle enzyme testing (CK and AST) – this can be done through a basic chemistry panel with your primary care vet

• Feed quality analysis and adjustment with a PSSM1 savvy equine functional nutrition professional

Quarterly Reviews:

• Complete veterinary physical examination and bloodwork

• Vitamin E and selenium testing (both are essential as they are co-factors to each other.)

• Management protocol effectiveness consideration

• Goal adjustment and long-term planning

The Genetic Counseling Conversation

One of the hardest parts of my job is discussing breeding implications with owners of PSSM1 horses. These are often valuable animals with exceptional bloodlines, and the genetic reality can be difficult to accept.

The Inheritance Facts: PSSM1 follows a dominant inheritance pattern - This means a horse only needs to inherit one copy of the mutated gene from either parent to be affected, unlike recessive conditions that require two copies.

Affected horses pass the mutation to 50% of their offspring - Every time an affected horse is bred, there's a coin-flip chance each foal will inherit the mutation and develop PSSM1.

Horses with two copies (homozygous) are typically more severely affected - These horses inherited the mutation from both parents and usually show more frequent and severe episodes than horses with just one copy.

The mutation doesn't skip generations - If a horse has PSSM1, at least one parent must also carry the mutation. However, some carriers may show such mild symptoms that the condition goes unrecognized until genetic testing is performed.

My Recommendations: Test all breeding stock before making any breeding decisions - Know the genetic status of both the mare and stallion before breeding to avoid producing affected foals.

Avoid breeding PSSM1-positive horses - The most responsible approach is to remove affected animals from breeding programs to prevent passing the mutation to future generations.

Plan for lifelong management costs in any offspring should you decide to breed - Affected foals will require specialized feeding, exercise protocols, and potentially higher veterinary costs throughout their lives. Budget accordingly before breeding and consider the difficulty in re-homing and/or selling affected offspring.

The Management Reality and Rewards

PSSM1 horses require lifelong attention to diet, exercise, and stress management, but many become exceptional athletes and companions when properly managed. Their genetic challenge often develops superior horsemanship skills and deeper partnerships.

Keys to Long-Term Success:

• Early diagnosis and intervention before severe episodes occur

• Owner commitment to daily protocols throughout the horse's life

• Professional team support from veterinarians, nutritionists, and trainers

• Realistic expectations about performance capabilities

Critical Mistakes to Avoid:

• Assuming initial improvement means the horse is "cured"

• Allowing complete rest days or returning to high-carbohydrate feeding

• Ignoring subtle warning signs of returning episodes

Owners who embrace these lifelong management requirements often develop stronger relationships with their horses and superior horsemanship skills compared to those managing horses without special needs. The intensive care required frequently results in better overall horse management that benefits their entire program.

Question? Concerns? Need help with your PSSM1 horse? Send us a message or join our mailing list for tips and tricks as well as updates on our upcoming book release:

Equine Muscle Disorders: The Functional Nutrition Revolution

A comprehensive guide to PSSM1 & PSSM2/MIM, MFM, and HYPP management

References:

Core Genetic and Pathophysiology Research

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Baird, J. D., Valberg, S. J., Anderson, S. M., McCue, M. E., & Mickelson, J. R. (2010). Presence of the glycogen synthase 1 (GYS1) mutation causing type 1 polysaccharide storage myopathy in continental European draught horse breeds. Veterinary Record, 167(20), 781-784. https://doi.org/10.1136/vr.c5597

Finno, C. J., Gianino, G., Perumbakkam, S., Williams, Z. J., Bordbari, M. H., Gardner, K. L., ... & Bannasch, D. L. (2018). A missense mutation in the skeletal muscle chloride channel (CLCN1) as candidate causal mutation for congenital myotonia in a New Forest pony. Neuromuscular Disorders, 28(7), 606-612. https://doi.org/10.1016/j.nmd.2018.04.011

McCoy, A. M., Schaefer, R., Petersen, J. L., Morrell, P. L., Slamka, M. A., Mickelson, J. R., ... & McCue, M. E. (2014). Evidence of positive selection for a glycogen synthase (GYS1) mutation in domestic horse populations. Journal of Heredity, 105(2), 163-172. https://doi.org/10.1093/jhered/est075

McCue, M. E., Armién, A. G., Lucio, M., Mickelson, J. R., & Valberg, S. J. (2009). Comparative skeletal muscle histopathologic and ultrastructural features in two forms of polysaccharide storage myopathy in horses. Veterinary Pathology, 46(6), 1281-1291. https://doi.org/10.1354/vp.08-VP-0177-M-FL

McCue, M. E., Valberg, S. J., Lucio, M., & Mickelson, J. R. (2008). Glycogen synthase 1 (GYS1) mutation in diverse breeds with polysaccharide storage myopathy. Journal of Veterinary Internal Medicine, 22(5), 1228-1233. https://doi.org/10.1111/j.1939-1676.2008.0167.x

McCue, M. E., Valberg, S. J., Miller, M. B., Wade, C., DiMauro, S., Akman, H. O., & Mickelson, J. R. (2008). Glycogen synthase (GYS1) mutation causes a novel skeletal muscle glycogenosis. Genomics, 91(5), 458-466. https://doi.org/10.1016/j.ygeno.2008.01.011

McCue, M. E., Valberg, S. J., Jackson, M., Lucio, M., Borgia, L., & Mickelson, J. R. (2009). Polysaccharide storage myopathy phenotype in Quarter Horse-related breeds is modified by the presence of an RYR1 mutation. Neuromuscular Disorders, 19(1), 37-43. https://doi.org/10.1016/j.nmd.2008.09.018

Stanley, R. L., McCue, M. E., Valberg, S. J., Mickelson, J. R., Mayhew, I. G., McGowan, C., ... & Piercy, R. J. (2009). A glycogen synthase 1 mutation associated with equine polysaccharide storage myopathy and exertional rhabdomyolysis occurs in a variety of UK breeds. Equine Veterinary Journal, 41(6), 597-601. https://doi.org/10.2746/042516409x407611

Tosi, I., Art, T., Cassart, D., Farnir, F., Ceusters, J., Serteyn, D., ... & Votion, D. M. (2018). Altered mitochondrial oxidative phosphorylation capacity in horses suffering from polysaccharide storage myopathy. Journal of Bioenergetics and Biomembranes, 50(5), 379-390. https://doi.org/10.1007/s10863-018-9768-6

Biochemical Mechanisms and Enzyme Function

Lewis-Smith, D., Goadsby, P. J., Pender, S., Sisodiya, S. M., Kullmann, D. M., & Waxman, S. G. (2017). A highly prevalent equine glycogen storage disease is explained by constitutive activation of a mutant glycogen synthase. Scientific Reports, 7(1), 13454. https://doi.org/10.1038/s41598-017-13919-1

Naylor, R. J., Livesey, L., Schumacher, J., Henley, W., Harris, P. A., & Piercy, R. J. (2012). Allele copy number and underlying pathology are associated with subclinical severity in equine type 1 polysaccharide storage myopathy (PSSM1). PLoS One, 7(8), e42317. https://doi.org/10.1371/journal.pone.0042317

Valberg, S. J., McCue, M. E., Mickelson, J. R., Lewis, S. S., Lavoie, J. P., & Shelton, J. (2017). Clinical characteristics and muscle glycogen concentrations in warmblood horses with polysaccharide storage myopathy. American Journal of Veterinary Research, 78(11), 1305-1312. https://doi.org/10.2460/ajvr.78.11.1305

Dietary Management and Nutritional Research

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De La Corte, F. D., Valberg, S. J., MacLeay, J. M., Williamson, S. E., & Mickelson, J. R. (1999). Glucose uptake in horses with polysaccharide storage myopathy. American Journal of Veterinary Research, 60(4), 458-462.

Harris, P. A., & Geor, R. J. (2009). Primer on dietary carbohydrates and utility of the glycemic index in equine nutrition. Veterinary Clinics of North America: Equine Practice, 25(1), 23-37. https://doi.org/10.1016/j.cveq.2009.01.003

Pagan, J. D., & Harris, P. A. (1999). The effects of timing and amount of forage and grain on exercise response in Thoroughbred horses. Equine Veterinary Journal, 31(S30), 451-457. https://doi.org/10.1111/j.2042-3306.1999.tb05259.x

Valentine, B. A., & Cooper, B. J. (2005). Incidence of polysaccharide storage myopathy: necropsy study of 225 horses. Veterinary Pathology, 42(6), 823-827. https://doi.org/10.1354/vp.42-6-823

Exercise Physiology and Management

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McKenzie, E. C., Valberg, S. J., Godden, S. M., Pagan, J. D., MacLeay, J. M., & Geor, R. J. (2003). Effect of oral administration of corticosteroids on concentrations of glucose, insulin, and cortisol in horses. American Journal of Veterinary Research, 64(1), 7-13. https://doi.org/10.2460/ajvr.2003.64.7

Rivero, J. L. L., & Piercy, R. J. (2013). Muscle histopathology in horses with polysaccharide storage myopathy type 1. Equine Veterinary Journal, 45(5), 612-618. https://doi.org/10.1111/evj.12028

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Vitamin E and Antioxidant Research

Bookbinder, L., Finno, C. J., Firshman, A. M., Katzman, S. A., Burns, E., Peterson, J., ... & Valberg, S. J. (2019). Impact of alpha-tocopherol deficiency and supplementation on sacrocaudalis and gluteal muscle fiber histopathology and morphology in horses. Journal of Veterinary Internal Medicine, 33(6), 2770-2779. https://doi.org/10.1111/jvim.15643

Brown, J. C., Valberg, S. J., Hogg, M., & Finno, C. J. (2017). Effects of feeding two RRR-α-tocopherol formulations on serum, cerebrospinal fluid and muscle α-tocopherol concentrations in horses with subclinical vitamin E deficiency. Equine Veterinary Journal, 49(6), 753-758. https://doi.org/10.1111/evj.12709

Fagan, M. M., Harris, P., Adams, A., Pazdro, R., Krotky, A., Call, J., ... & Urschel, K. L. (2017). Form of vitamin E supplementation affects oxidative and inflammatory response in exercising horses. Journal of Equine Veterinary Science, 58, 80-89. https://doi.org/10.1016/j.jevs.2017.08.010

Williams, C. A., & Carlucci, S. A. (2006). Oral vitamin E supplementation on oxidative stress, vitamin and antioxidant status in intensely exercised horses. Equine Veterinary Journal, 38(S36), 617-621. https://doi.org/10.1111/j.2042-3306.2006.tb05601.x

Selenium and Mineral Research

Combs, G. F. (2001). Selenium in global food systems. British Journal of Nutrition, 85(5), 517-547. https://doi.org/10.1079/BJN2000280

Geor, R. J., & Harris, P. (2009). Dietary management of obesity and insulin resistance: countering risk for laminitis. Veterinary Clinics of North America: Equine Practice, 25(1), 51-65. https://doi.org/10.1016/j.cveq.2009.01.009

Richardson, S. M., Siciliano, P. D., Engle, T. E., Larson, C. K., & Ward, T. L. (2006). Effect of selenium supplementation and source on the selenium status of horses. Journal of Animal Science, 84(7), 1742-1748. https://doi.org/10.2527/jas.2005-413

Inheritance Patterns and Genetics

Beeson, S. K., Mickelson, J. R., & McCue, M. E. (2019). Exploration of fine-scale recombination rate variation in the domestic horse. Genome Research, 29(10), 1744-1752. https://doi.org/10.1101/gr.243311.118

Herszberg, B., McCue, M. E., Larcher, T., Mata, X., Vaiman, A., Chaffaux, S., ... & Guérin, G. (2009). A GYS1 gene mutation is highly associated with polysaccharide storage myopathy in Cob Normand draught horses. Animal Genetics, 40(1), 94-96. https://doi.org/10.1111/j.1365-2052.2008.01799.x

Johlig, L., Valberg, S. J., Mickelson, J. R., Klukowska, J., Reusser, H. R., Straub, R., & Gerber, V. (2011). Epidemiological and genetic study of exertional rhabdomyolysis in a Warmblood horse family in Switzerland. Equine Veterinary Journal, 43(2), 240-245. https://doi.org/10.1111/j.2042-3306.2010.00271.x

Tryon, R. C., Penedo, M. C. T., McCue, M. E., Valberg, S. J., Mickelson, J. R., Famula, T. R., ... & Bannasch, D. L. (2009). Allele frequencies of inherited disease genes in subpopulations of American Quarter Horses. Journal of the American Veterinary Medical Association, 234(1), 120-125. https://doi.org/10.2460/javma.234.1.120

PSSM2 and Related Myopathies Research

Lewis, S. S., Valberg, S. J., & Nielsen, I. L. (2017). Muscle glycogen concentrations and response to diet and exercise regimes in Warmblood horses with type 2 polysaccharide storage myopathy. PLoS One, 12(9), e0184773. https://doi.org/10.1371/journal.pone.0184773

Valberg, S. J., Lewis, S. S., Shivers, J. L., Barnes, N. E., Konczak, J. S., Draper, A. C., ... & McCue, M. E. (2015). The equine movement disorder "shivers" is associated with selective cerebellar Purkinje cell axonal degeneration. Veterinary Pathology, 52(6), 1087-1098. https://doi.org/10.1177/0300985815571668

Clinical Management Studies

Firshman, A. M., Baird, J. D., & Valberg, S. J. (2005). Prevalences and clinical signs of polysaccharide storage myopathy and shivers in Belgian draft horses. Journal of the American Veterinary Medical Association, 227(10), 1694-1699. https://doi.org/10.2460/javma.2005.227.1694

Valberg, S. J., Ward, T. L., Rush, B., Kinde, H., Hiraragi, H., Nahey, D., ... & Sissom, E. (2001). Glycogen branching enzyme deficiency in quarter horse foals. Journal of Veterinary Internal Medicine, 15(6), 572-580. https://doi.org/10.1111/j.1939-1676.2001.tb01590.x

Ward, T. L., Valberg, S. J., Adelson, D. L., Pacciotti, A., Godard, S., & Marty, G. (2004). Glycogen branching enzyme (GBE1) mutation causing equine glycogen storage disease IV. Mammalian Genome, 15(7), 570-577. https://doi.org/10.1007/s00335-004-2369-1

Review Articles and Guidelines

Finno, C. J., & Valberg, S. J. (2012). A comparative review of vitamin E and associated equine disorders. Journal of Veterinary Internal Medicine, 26(6), 1251-1266. https://doi.org/10.1111/j.1939-1676.2012.00994.x

Geor, R. J. (2008). Metabolic predispositions to laminitis in horses and ponies: obesity, insulin resistance and metabolic syndromes. Journal of Equine Veterinary Science, 28(12), 753-759. https://doi.org/10.1016/j.jevs.2008.10.016

Valberg, S. J. (2018). Muscle conditions affecting sport horses. Veterinary Clinics of North America: Equine Practice, 34(2), 253-276. https://doi.org/10.1016/j.cveq.2018.04.004